Saturday, November 13, 2010

DNA Says Evolution is Not as Contingent as Imagined

(Darwin Isn’t Dead. He Just Smells Funny.*)
*Apologies to FZ

Something funny is afoot in the biological sciences. Labs peering into DNA are seeing things that nobody expected. And because the received view of evolution failed to predict these findings, and because it has little room to incorporate them, a crisis is brewing for the theory. Something more than selecting random variants is going on in evolution.

The data coming out of DNA sequencing and analysis suggest that the something more has to do with a preferred direction in evolution. Phylogenetic descent seems now to be a developmental unfolding. Several discoveries point to this conclusion:

1. Junk DNA. This is not a particularly new discovery. It’s been known for some time that all species carry around a lot of junk, DNA that appears to lie dormant. What aspect of evolution theory predicts that long stretches of inactive DNA would coast along inside organisms, seemingly contributing nothing to their survivability? Nobody saw it coming. It was an empirical surprise.

But in the context of ontogeny, the development of organisms, it is exactly what is to be expected. Each cell in the body of a complex organism inherits the same genes from the ancestral zygote, the original fertilized ovum. Despite all possessing the same genes, brain, liver, kidney, and skin cells, for example, distinguish themselves phenotypically. Each cell type looks and acts differently from the others. But, because they all inherit the same genes, there must be a lot of junk DNA in each type of cell. Brain cells don’t need genes that function uniquely in liver cells, nor do kidney cells need genes that function uniquely in skin cells. But all the cells inherit all those genes from their common ancestor, the zygote, whether they need them or not.

When it comes to cell types in a body, an invariant genetic inheritance necessarily is the case, with lots of junk in each cell as a result. Ontogeny demonstrates that diverse morphologies, or phenotypes, need not correspond to any proportionate diversity of genotype. “Adaptive radiation” of cell types in a body proceeds just fine without genetic variation.

Evolution appears to operate similarly.

2. Conservation of DNA. Genetic material across species, though not invariant, turns out to be much less variable than observable differences among species would suggest. DNA is highly conserved across species. In their article, Regulating Evolution (Scientific American, May 2010) researchers Sean B. Carroll, Benjamin Prud’homme, and Nicolas Gompel comment,
For a long time, scientists certainly expected the anatomical differences among animals to be reflected in clear differences among the contents of their genomes. When we compare mammalian genomes such as those of the mouse, rat, dog, human and chimpanzee, however, we see that their respective gene catalogues are remarkably similar. [. . . .] When comparing mouse and human genomes, for example, biologists are able to indentify a mouse counterpart of at least 99 percent of all our genes.
The perplexed authors elaborate on the new findings:
. . . to our surprise, it has turned out that differences in appearance are deceiving: very different animals have very similar sets of genes.
The preservation of coding sequences over evolutionary time is especially puzzling when one considers the genes involved in body building and body patterning.
The discovery that body-building proteins are even more alike on average than other proteins was especially intriguing because of the paradox it seemed to pose: animals as different as a mouse and an elephant are shaped by a common set of very similar, functionally indistinguishable body-building proteins.
Surprise? Puzzling? Paradox? Why does evolution theory suffer so many bouts of the unexpected now that genomes are yielding their secrets? If the received theory of evolution were solid, wouldn’t new genetic details have slots waiting for them in it? Shouldn’t new genetic data bolster the theory, rather than generate surprises, puzzles and paradoxes for it to resolve?

Why didn’t evolution theorists predict that phenotypic and genotypic differences across species would turn out to be so disproportionate, that so few genes would produce so many species? Nobody saw it coming. It was an empirical surprise.

3. Genetic switches. The differentiation of cell types in a developing organism is managed by homeobox genes. These genes function as master “switches” that trigger the expression and repression of other genes. By selectively turning other genes on and off at various stages of development, homeobox genes effectively control the varieties of tissues that will populate a body. This oversight function partly answers the riddle of junk DNA. Some genes that can appear dormant actually code for proteins whose phenotypic activity is the modulation of other genes. The regulatory genes are not junk.

Now, due to the work of Carroll, Prud’homme, Gompel and others, it looks like evolution uses regulatory genes in the same way.

Instead of spinning off variant cell types, the cycling on and off of genetic switches in the context of evolution spins off variant species. This discovery, of the importance of genetic switches in evolution and its helping to account for the low level of genetic diversity across species, was an empirical surprise. Nobody saw it coming.

The explanatory power of this discovery has produced a new discipline within evolutionary biology, called evolutionary developmental biology, or evo-devo, a science that gives regulatory genes a starring role in evolution.

4. Anticipatory genes. A new organism, a zygote, a fertilized egg carries many genes that ride along unexpressed—until they are needed by descendant cell types. The zygote anticipates, in its genetic catalog, the genes that remote descendant cells will need, even if those genes contribute nothing to the survival of the zygote itself or its immediate descendants. The zygote divides into two cells, and the two into four, and the four into eight, and so on. The cells that make up these early stages are said to be totipotent cells—they can bear descendants of any cell type. Later, after a degree of specialization, cells become pluripotent—they can give rise to several cell types, though not to all. And the specialization continues from there, with descendants inheriting from their ancestors the specialized genes they need, along with the rest of the genome.

This is to be expected in the context of a developing organism.

But it turns out that ancient species also carry genes that seem to anticipate the needs of descendants. A news article in Nature covering the sequencing of the genome of the Great Barrier Reef sponge Amphimedon queenslandica, reveals that the hoary creatures harbor a “tookit” of metazoan genes:
The genome also includes analogues of genes that, in organisms with a neuromuscular system, code for muscle tissue and neurons.
A curious finding. The article continues:
According to Douglas Erwin, a palaeobiologist at the Smithsonian Institution in Washington DC, such complexity indicates that sponges must have descended from a more advanced ancestor than previously suspected. "This flies in the face of what we think of early metazoan evolution," says Erwin.
Charles Marshall, director of the University of California Museum of Paleontology in Berkeley, agrees. "It means there was an elaborate machinery in place that already had some function," he says. "What I want to know now is what were all these genes doing prior to the advent of sponges.
The conundrum for normal evolution theory is clear. But, rather than propose that the genes needed by organisms with neuromuscular systems are in the sponge for the anticipatory purpose of providing those genes to descendants who will need them, the scientists invent an imaginary ancestor of the sponge that needed the genes. But the ghostly ancestor would have had to have arisen within a very narrow window. Fossil evidence of sponges goes back 650 million years; it constitutes, the authors note, “the oldest evidence for metazoans (multicellular animals) on Earth.” So, what use would any species even more primitive than sponges have for the neuromuscular genes? Nobody saw it coming. It was an empirical surprise.

But the sponge genome is only one example. Research is finding case after case of ancestral species that harbor genes essential for remote descendants. Another example: It turns out that a species of unicellular protozoan carries genes essential for metabolic processes specific to metazoans. The researchers who discovered the surprise genes and published their data (PNAS – 2010 107 (22) 10142-10147) explain,
One of the most important cell adhesion mechanisms for metazoan development is integrin-mediated adhesion and signaling. The integrin adhesion complex mediates critical interactions between cells and the extracellular matrix, modulating several aspects of cell physiology. To date this machinery has been considered strictly metazoan specific. [. . . .] Unexpectedly, we found that core components of the integrin adhesion complex are encoded in the genome of the apusozoan protist Amastigomonas sp., and therefore their origins predate the divergence of Opisthokonta, the clade that includes metazoans and fungi. [. . . .] Our data highlight the fact that many of the key genes that had formerly been cited as crucial for metazoan origins have a much earlier origin (emphasis added).
And the surprises just keep coming.
A news release (11/24/2005) issued by the journal Trends in Genetics announces that
Corals and sea anemones (the flowers of the sea), long regarded as merely simple sea-dwelling animals, turn out to be more genetically complex than first realised. They have just as many genes as most mammals, including humans, and many of the genes that were thought to have been "invented" in vertebrates are actually very old and are present in these "simple" animals.
The full text of the release is available at ch/technau_Science.pdf
Newer (2007) sequencing and analysis results corroborate the anemone anomalies.

Another example comes from research at the European Molecular Biology Laboratory, which found human genes in a marine worm. The news release (11/24/2005) announcing the discovery is at ia_relations/2005/051124_heidelberg/index.html

Additional research has found that genes essential for human nerve cells to communicate with one another are present already in bacteria. This research is described in a NIH news release (6/1/2004) at

What is particularly striking about these findings, taken together—and what is particularly interesting to the star larvae hypothesis—is not only that they were unanticipated by the practitioners who engineered the current theory, but also that they make the evolutionary process look an awful lot like a developmental process, like a stage, or stages, in the life cycle of a developing organism. 
The findings are paradoxical only for a theory that sees evolution as pure contingency. If evolution is recognized as the developmental unfolding of a life cycle, then the findings
  • that much of its genome is unexpressed in any particular species,
  • that phenotypic variation dwarfs genotypic variation (DNA is conserved),
  • that genetic switches play key regulatory roles in phylogenetic descent and
  • that ancestors carry genes needed in the future by remote descendants
are to be expected, because they are what we find when we study the differentiation of cells types in complex organisms.

To propose that evolution is programmed in a way similar to that in which the development of an organism is programmed is anathema to current evolution theory. The current theory has no room for teleology. But the new research findings point directly to such a conclusion. As happens in the history of science, scientists have to decide whether to stretch the normal paradigm to try to cover a growing collection of anomalous data or to construct a new paradigm based on the data.

And as soon as the dust settles on that biological revolution, a new funniness will be afoot. It already is. Quantum genetics, anyone?